USP16 S-nitrosylation aggravates coronary microembolization-induced myocardial injury via repressing KDM1A-mediated glutathione homeostasis

Inhibition of SNO-USP16 at the C731 site represses ubiquitination and degradation of KDM1A protein to epigenetically activate GCLM and GLS, which maintains GSH homeostasis and relieves CME-induced myocardial injury.